Age-specific cancer rates show large historical increases that indict environmental risk factors. But these environmental factors did not necessarily act by increasing oncomutation rates. Mathematical analyses suggest selective effects on preexisting oncomutants. The widely held hypothesis that environmental chemicals induce a substantial fraction of human point mutations has not been supported by observation. Direct measurement of the kinds and numbers of point mutations in human tissues have, in fact, found no clear relationship with exposure to environmental agents, save for sunlight in the skin. Alternative hypotheses that point mutations arise primarily as errors during turnover of undamaged DNA and that environmental conditions select rather than induce oncomutants seem to better explain the facts of environmental carcinogenesis in humans.
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